These data support earlier research and anecdotal observations of a substantial sleep/migraine relationship, and implicate sleep disturbance in specific headache patterns and severity. The short sleep group, who routinely slept 6 hours per night, exhibited the more severe headache patterns and more sleep-related headache. Sleep complaints occurred with greater frequency among chronic than episodic migraineurs. Future research may identify possible mediating factors such as primary sleep and mood disorders. Prospective studies are needed to determine if normalizing sleep times in the short sleeps would impact headache threshold.

The objective of this study was to evaluate the time-series relationships between stress, sleep duration, and headache pain among patients with chronic headaches. Sleep and stress have long been recognized as potential triggers of episodic headache (< 15 headache days/month), though prospective evidence is inconsistent and absent in patients diagnosed with chronic headaches (≥ 15 days/month). We reanalyzed data from a 28-day observational study of chronic migraine (n = 33) and chronic tension-type headache (n = 22) sufferers. Patients completed the Daily Stress Inventory and recorded headache and sleep variables using a daily sleep/headache diary. Stress ratings, duration of previous nights' sleep, and headache severity were modeled using a series of linear mixed models with random effects to account for individual differences in observed associations. Models were displayed using contour plots. Two consecutive days of either high stress or low sleep were strongly predictive of headache, whereas two days of low stress or adequate sleep were protective. When patterns of stress or sleep were divergent across days, headache risk was increased only when the earlier day was characterized by high stress or poor sleep. As predicted, headache activity in the combined model was highest when high stress and low sleep occurred concurrently during the prior 2 days denoting an additive effect. Future research is needed to expand on current findings among chronic headache patients and to develop individualized models that account for multiple simultaneous influences of headache trigger factors.

Theoretical developments and burgeoning research on stress and illness in the mid-20th century yielded the foundations necessary to conceptualize headache as a psychophysiological disorder and eventually to develop and apply contemporary behavioral headache treatments. Over the past three decades, these behavioral headache treatments (relaxation training, biofeedback, cognitive-behavioral therapy, and stress-management training) have amassed a sizeable evidence base. Meta-analytic reviews of the literature consistently have shown behavioral interventions to yield 35% to 55% improvements in migraine and tension-type headache and that these outcomes are significantly superior to control conditions. The strength of the evidence has lead many professional practice organizations to recommend use of behavioral headache treatments alongside pharmacologic treatments for primary headache. The present overview was prepared as a companion article to and intended to provide a background for the Guidelines for Trials of Behavioral Treatments for Recurrent Headache also published within this journal supplement. This article begins with a synopsis of key historical developments leading to our current conceptualization of migraine and tension-type headache as psychophysiological disorders amenable to behavioral intervention. The evolution of the behavioral headache literature is discussed, exemplified by publication trends in the journal Headache. Leading empirically-based behavioral headache interventions are described, and meta-analytic reviews examining the migraine and tension-type headache literatures are summarized, compared, and contrasted. A critique of the methodological quality of the clinical trials literature is presented, highlighting the strengths and weaknesses in relation to recruitment and selection of patients, sample size and statistical power, the use of a credible control, and the reproducibility of the study interventions in clinical practice.

The comorbidity of headache and psychiatric disorders is a well-recognized clinical phenomenon warranting further systematic research. Affective disorders occur with at least three-fold greater frequency among migraineurs than among the general population, and the prevalence increases in clinical populations, especially with chronic daily headache. When present, psychiatric comorbidity complicates headache management and portends a poorer prognosis for headache treatment. However, the relationship between headache and psychopathology has historically been misunderstood, and Headache has been associated with psychiatric illness in the medical literature for well over a century. Unfortunately, as noted by Silberstein and colleagues, 1 the relationship between headache and psychopathology has been clinically discussed far more often than it has been systematically studied. This relationship remains probably one of the most poorly understood, while at the same time clinically important, areas for future headache research. The present article provides a brief historical context for research examining headache and psychiatric comorbidity. Despite an arguably dubious genesis emerging from psychoanalytic case reports with little evidence supporting 493

Depressed subjects (N = 31) were treated with three different group therapies: (a) complete cognitive therapy (CCT); (b) partial cognitive therapy (PCT); or (c) comprehensive distancing (CD). All three groups showed significant, but equivalent, reductions in depression over 12 weeks of treatment and 2-month follow-up. However, significant reductions in dysfunctional attitudes obtained for CCT and PCT were not found for CD, which suggests different underlying therapeutic processes. Comparisons with other studies noted no differences in the efficacy of CT as a function of treatment format, but a trend toward reduced effectiveness for group vs. individual CD.

Review of epidemiological and clinical studies suggests that sleep disorders are disproportionately observed in specific headache diagnoses (eg, migraine, tension-type, cluster) and other nonspecific headache patterns (ie, chronic daily headache, "awakening" or morning headache). Interestingly, the sleep disorders associated with headache are of varied types, including obstructive sleep apnea (OSA), periodic limb movement disorder, circadian rhythm disorder, insomnia, and hypersomnia. Headache, particularly morning headache and chronic headache, may be consequent to, or aggravated by, a sleep disorder, and management of the sleep disorder may improve or resolve the headache. Sleep-disordered breathing is the best example of this relationship. Insomnia is the sleep disorder most often cited by clinical headache populations. Depression and anxiety are comorbid with both headache and sleep disorders (especially insomnia) and consideration of the full headache-sleep-affective symptom constellation may yield opportunities to maximize treatment. This paper reviews the comorbidity of headache and sleep disorders (including coexisting psychiatric symptoms where available). Clinical implications for headache evaluation are presented. Sleep screening strategies conducive to headache practice are described. Consideration of the spectrum of sleep-disordered breathing is encouraged in the headache population, including awareness of potential upper airway resistance syndrome in headache patients lacking traditional risk factors for OSA. Pharmacologic and behavioral sleep regulation strategies are offered that are also compatible with treatment of primary headache.

Guidelines for design of clinical trials evaluating behavioral headache treatments were developed to facilitate production of quality research evaluating behavioral therapies for management of primary headache disorders. These guidelines were produced by a Workgroup of headache researchers under auspices of the American Headache Society. The guidelines are complementary to and modeled after guidelines for pharmacological trials published by the International Headache Society, but they address methodologic considerations unique to behavioral and other nonpharmacological treatments. Explicit guidelines for evaluating behavioral headache therapies are needed as the optimal methodology for behavioral (and other nonpharmacologic) trials necessarily differs from the preferred methodology for drug trials. In addition, trials comparing and integrating drug and behavioral therapies present methodological challenges not addressed by guidelines for pharmacologic research. These guidelines address patient selection, trial design for behavioral treatments and for comparisons across multiple treatment modalities (eg, behavioral vs pharmacologic), evaluation of results, and research ethics. Although developed specifically for behavioral therapies, the guidelines may apply to the design of clinical trials evaluating many forms of nonpharmacologic therapies for headache.

Several articles have recently questioned the distinction between acceptance and commitment therapy (ACT) and traditional cognitive therapy (CT). This study presents a reanalysis of data from Zettle and Rains that compared 12 weeks of group CT with group ACT. For theoretical reasons, Zettle and Rains also included a modified form of CT that did not include distancing, and no intent-to-treat analysis was included. Particularly because that unusual third condition did somewhat better than the full CT package, it contaminated the direct comparison of ACT and CT, which has of late become theoretically interesting. In the present study, data from participants in the ACT and CT conditions were reanalyzed. ACT was shown to produce greater reductions in levels of self-reported depression using an intent-to-treat analysis. Posttreatment levels of cognitive defusion mediated this effect at follow-up. The occurrence of depressogenic thoughts and level of dysfunctional attitudes did not function as mediators. This study adds additional evidence that ACT works through distinct and theoretically specified processes that are not the same as CT.